In general, the activities of various enzymes within bodily fluids, such as the blood or lymph, are of clinical interest. Some enzymes exist in bodily fluids as an inactive precursor until an event or condition triggers their activation. For example, the enzymes kallikrein and thrombin are present in blood as their respective inactive precursors, prekallikrein and prothrombin, until activated. The activation of enzymes, such as kallikrein and thrombin, can indicate clinically significant underlying events or conditions.
Kallikrein is involved in the processes of signaling painful events or stimuli to the nervous system via the extrinsic pain pathway. When an agent, such as heat, force, or radiation, causes a cell to rupture, that cell releases its internal components into the surrounding environment. Among these cell components are proteins that activate kallikrein, i.e., convert inactive prekallikrein to kallikrein. Kallikrein in turn activates a protein called bradykinin, which acts on free nerve endings to signal pain in the area. Bradykinin can also induce pain by causing tissue to swell, e.g. by causing edema.
Thrombin is involved in the process of blood coagulation. Specifically, thrombin converts fibrinogen into fibrin, which in turn forms thrombi. Prothrombin is converted to thrombin as part of an intricate cascade of enzymatic activities. Generally speaking, patients with conditions that lead to pooling of the blood within vessels, such as atrial fibrillation, or patients with implanted foreign matter exposed to blood flow, such as artificial heart valves, are at increased risk of developing potentially life-threatening thrombi. Such patients often receive anticoagulants to reduce the likelihood of thrombus formation.